This invention relates to a method for treating cardiac insufficiency in warm-blooded mammals. In particular it relates to a method for enhancing the contractile force of mammalian cardiac muscle which comprises administering an effective amount of the antibiotic A-23187.
The stimulation of cardiac muscle in clinical situations producing cardiogenic shock, for example following myocardial infarction or in congestive heart failure, is clinically achieved by the administration of inotropic agents such as isoproterenol or other known cardioactive agents. Some of these agents act by releasing endogenous norepinephrine which in turn stimulates the heart muscle. Others, e.g., isoproterenol, act as agonists of .beta.-receptors. Each of these mechanisms of action carries with it undesirable side reactions necessitating careful clinical observation. For example, the release of endogenous norepinephrine causes an increase in peripheral resistance which in turn places an additional undesirable burden on the heart.
There is a continuing need for more effective positive inotropic agents which do not act through release of endogenous norepinephrine or which are not agonists of .beta.-receptors.